Study of the effect of inactivating previously activated neurons in the hippocampus during repeated chronic stress in c-fos-lacZ transgenic rats on the habituation process of autonomic, neuroendocrine and neuroinflammatory responses.

• Grant number: 23/00306-4
• Support Opportunities: Scholarships in Brazil - Doctorate (Direct)
• Start date: March 01, 2023
• End date: January 31, 2027
• Field of knowledge: Biological Sciences - Pharmacology - Neuropsychopharmacology
• Principal Investigator: Cristiane Busnardo Santiago
• Grantee: Luana Omena Giatti
• Host Institution: Faculdade de Ciências Farmacêuticas (FCFAR). Universidade Estadual Paulista (UNESP). Campus de Araraquara. Araraquara , SP, Brazil
• Associated research grant: 18/04899-1 - GENETIC STUDY OF HYPOCAMPUS GLUTAMATE NEUROTRANSMISSION IN CENTRAL MECHANISMS OF THE ADAPTATION OF NEUROENDOCRINE, CARDIOVASCULAR AND BEHAVIORAL RESPONSES TO REPEATED CHRONIC STRESS AND STRESS-INDUCED NEUROINFLAMATION, AP.JP
• Associated scholarship(s): 23/15852-4 - Role of Hippocampal-Hindbrain Circuitry in Stress Habituation in Male and Female Rats, BE.EP.DD

Abstract

Emotional stress causes a physiological and psychological imbalance in the body and it has been associated with several pathologies, including cardiovascular diseases and psychiatric disorders. Stressful stimuli cause cardiovascular changes, characterized by an increase in mean arterial pressure (MAP) and heart rate (HR), and HPA axis activation , with increases in corticosterone and adrenocorticotropin (ACTH) plasma levels and accompanied by emotional consequences, such as anxiety disorders and depression. Furthermore, glucocorticoids and neurotransmitters (e.g. glutamate) released during stressful situations induce pro-inflammatory cytokines release and expression of their receptors. Prolonged or repeated exposure to real or potential threats initiates adaptive processes aimed at minimize the impact of stress on the body. However, despite the importance of stress responses habituation, the neurobiological and neurochemical mechanisms involved in this process are still poorly understood. Therefore, the hypothesis of the present project is that repeated chronic stress-related autonomic, neuroendocrine, neuroinflammatory adaptations are mediated by hippocampal neurons activation . For this, hippocampus neurons that were previously activated during stress will be selectively inactivated, through the Daun02 inactivation method in c-Fos lacZ transgenic rat.